In patients with SLE, exposure to indoxyl sulfate, a metabolite of tryptophan degradation, increases AhR activity in the periglomerular region and in the proximal and distal renal tubules, causing renal fibrosis characterized by podocyte injury, progressive glomerular damage, and a proinflammatory phenotype associated with LN39. This evidence concerns the gene AHR and renal fibrosis.